Chapter 8 / Heart Murmurs: Part II 275 8 Heart Murmurs Part II CONTENTS DIASTOLIC MURMURS DIASTOLIC MURMURS OF MITRAL ORIGIN DIASTOLIC MURMURS OF TRICUSPID ORIGIN SEMILUNAR VALVE REGURGITATION AORTIC REGURGITATION PULMONARY REGURGITATION CLINICAL ASSESSMENT OF DIASTOLIC MURMURS CONTINUOUS MURMURS PERSISTENT DUCTUS ARTERIOSUS AORTO-PULMONARY WINDOW SINUS OF VALSALVA ANEURYSM CORONARY ARTERIOVENOUS FISTULAE VENOUS HUM MAMMARY SOUFFLE CLINICAL ASSESSMENT OF CONTINUOUS MURMURS PERICARDIAL FRICTION RUB INNOCENT MURMURS REFERENCES DIASTOLIC MURMURS Diastolic murmurs can be caused by turbulent flow through the atrioventricular valves (the mitral and tricuspid valves) or turbulence caused by regurgitation of blood through the semilunar valves (the aortic and pulmonary valves). We will first discuss diastolic murmurs arising from turbulent flow through the atrioventricular valves. DIASTOLIC MURMURS OF MITRAL ORIGIN Turbulent flow across the mitral valve capable of producing a diastolic murmur can occur under the following conditions: • When there is increased pressure in the left atrium because of obstruction at the valve • When there is excessive volume of flow during diastole through the mitral valve with or without elevated left atrial pressure • Normal or increased mitral inflow velocity through a somewhat abnormal mitral valve • Normal mitral inflow through a functionally stenotic mitral orifice in the absence of organic valvular disease 275 276 Cardiac Physical Examination Fig. 1. Simultaneous recording of the left ventricular (LV) and the left atrial (LA) pressure curves obtained at cardiac catheterization from a patient with significant mitral stenosis. The rhythm is atrial fibrillation with varying diastolic intervals. A significant and persistent gradient through- out diastole is noted between the LA and the LV pressures even when the diastole is relatively long (e.g., following the fifth beat). Mitral Obstruction Secondary to Mitral Valvular Stenosis Mitral valvular obstruction may result from a congenitally stenosed valve or acquired stenosis such as caused by rheumatic heart disease where the leaflets are tethered and the commissures become fused because of the rheumatic process (1–4). Congenital mitral stenosis is rare, and when it occurs in combination with an atrial septal defect, the condition goes by the name of Lutembacher syndrome (5–7). Rarely, the obstruction may be caused by a left atrial tumor such as an atrial myxoma (8,9). An atrial myxoma is a benign tumor with a myxoid matrix of gelatinous consistency. It may be associated with constitutional symptoms, such as fever, and systemic inflammatory signs, such as elevated sedimentation rate. The myxoma is usually attached by a stalk to the interatrial septum and may prolapse into the ventricle in early diastole when the valve opens and cause obstruction to the mitral inflow. In the normal heart, the v wave pressure that is built up in the left atrium at the end of systole provides the gradient in early diastole for the diastolic flow to occur through the mitral valve. At this time the left ventricular pressure is close to zero. During the rapid filling phase of diastole, there is a fall in the left atrial pressure and a rise in the left ventricular diastolic pressure because of emptying of the left atrium and filling of the left ventricle, respectively. When there is any significant obstruction to flow at the mitral valve, the left atrial pressure will be elevated due to the obstruction, and the flow through the valve in diastole will occur under a higher v wave pressure gradient. The more severe the obstruction or the stenosis, the more persistent will be the elevation in the left atrial pressure. The pressure gradient between the left atrium and the left ven- tricle will tend to persist throughout diastole. The diastolic flow occurring under a higher and persistent pressure gradient will contribute to a turbulent flow, which may persist throughout diastole. The normal left atrial v wave pressure is usually about 12–15 mmHg. When there is significant mitral stenosis, the v wave pressure may be elevated up to 25–30 mmHg (Fig. 1). However, the pressure gradient noted even with severe mitral stenosis is still fairly low in terms of the absolute mmHg elevation. Chapter 8 / Heart Murmurs: Part II 277 On the other hand, the volume of flow through the mitral valve is always significant since the entire stroke volume of the heart will have to go through the mitral valve in diastole. Thus, a large volume going through the mitral valve under relatively low levels of pressure will be expected to give rise to turbulence, which will produce predominantly low-frequency murmur. In fact, the low pitch of the mitral stenosis murmur gives its characteristic rumbling quality on auscultation. The loudness of the murmur produced by the turbulence will depend to a certain extent on the adequacy of the cardiac output, whereas the length will depend more on the length of time the pressure gradient persists in diastole. The latter will tend to last throughout diastole when the stenosis is severe (1,3,10–13). CHARACTERISTICS OF MITRAL STENOSIS MURMURS The diastolic murmur of mitral stenosis will be expected to begin in diastole after the mitral valve opens and the rapid filling phase of diastole begins. The murmur is low pitched and often very well localized to the apex. The murmur may be so localized that unless one auscultates at the apex it may be missed. The best way to hear the murmur is to have the patient turn to the left lateral decubitus position and locate the left ventricular apex and use the bell to listen. The murmur has a rumbling quality and sounds like a distant roar of a thunder. The loud S1 and the opening snap following the S2, which are invariably present in classical mitral stenosis, give the background for auscultation. Together they make a cadence: One …..Two …ta r r r r r r r r The loudness of the murmur has no relationship to the severity of the stenosis. The loudness of the murmur may be related to the adequacy of the cardiac output. In severe pulmonary hypertension secondary to the mitral stenosis, the high pulmo- nary vascular resistance is usually associated with decreased cardiac output. In such patients with severe mitral stenosis and low-output symptoms the murmur may be soft and may even be inaudible. Occasionally in overdiuresed patients and decreased intra- vascular volume, the murmur may be soft despite significant stenosis. When the cardiac output is increased by slight exercise, such as walking for a few minutes, the murmur may be brought out more clearly. The length of the murmur has an important relationship to the severity of the mitral stenosis. If the stenosis is severe and is associated with a persistent diastolic gradient, the murmur will last throughout diastole until the beginning of next systole (Fig. 2). In atrial fibrillation the varying diastolic pauses provide a good opportunity to assess the length of the murmur in relation to the long pauses of diastole. The diastolic murmur of mitral stenosis will often have a presystolic crescendo to the loud M1 (Fig. 2) (14,15) . Occasionally one may hear only the presystolic murmur (Fig. 3). If this is the case, it usually means that the mitral stenosis is mild. The presystolic murmur tends to have some higher frequencies in that one can easily hear this with the chest piece of the stethoscope, unlike the diastolic rumble. Generally the presystolic murmur is not heard when the valve is heavily calcified and rigid. The left ventricle begins to contract at the end of diastole. When the left ventricular pressure exceeds the left atrial pressure, the mitral valve will close. The column of blood contained in the left ventricle, being moved by the contracting left ventricle, will be suddenly decelerated against the closed mitral valve, causing the loud M1. The loud- ness of M1 stems from the high dP/dt of the left ventricle at the time of closure of the 278 Cardiac Physical Examination Fig. 2. Simultaneous recording of eclectrocardiogram (ECG), carotid pulse (CP), apexcardiogram (Apex), and phonocardiogram (Phono) taken at the apex area from a patient with severe mitral stenosis. The Phono recording shows the full-length diastolic murmur, which begins immedi- ately following the opening snap (OS). The low-frequency murmur is initially loud and dimin- ishes slightly later to become accentuated with a crescendo shape ending with a loud intensity first heart sound (S1). The systole is free of murmur. Fig. 3. Simultaneous recording of electrocardiogram (ECG), carotid pulse (CP), apexcardiogram (Apex), and phonocardiogram (Phono) taken at the apex area from a patient with mild mitral stenosis. The Phono shows predominantly a presystolic murmur increasing in intensity ending with a large-amplitude first heart sound (S1). Note that the murmur has predominantly high frequency. mitral valve as a result of the elevated left atrial pressure. This has been discussed previously in relation to the S1. Although with sinus rhythm and preserved atrial contraction and relaxation one should expect a crescendo–decrescendo murmur with the increasing flow velocity associated with atrial contraction and decreasing flow velocity during atrial relaxation, Chapter 8 / Heart Murmurs: Part II 279 only the crescendo presystolic murmur is characteristic of mitral stenosis. Very rarely, when the PR interval is prolonged, one may observe and record a crescendo–decre- scendo murmur. Simultaneous recording of the left ventricular and left atrial pressures will show that the presystolic crescendo effect actually occurs at a time when the gradient is diminishing with the rising left ventricular pressure because of its contraction just before the crossover point of the pressures (4). In addition, the presystolic crescendo of the diastolic murmur can be recognized in shorter diastoles during atrial fibrillation (15). This would suggest that the increased volume and velocity of flow during the a wave rise in the left atrial pressure because of atrial systole in sinus rhythm alone is not adequate to explain its mechanism.